Chronic Toxoplasma gondii infection contributes to perineuronal nets impairment in the primary somatosensory cortex

Toxoplasma gondii is able to manipulate the host immune system to establish a persistent and efficient infection, contributing to the development of brain abnormalities with behavioral repercussions. In this context, this work aimed to evaluate the effects of T. gondii infection on the systemic inflammatory response and structure of the primary somatosensory cortex (PSC). C57BL/6 and BALB/c mice were infected with T. gondii ME49 strain tissue cysts and accompanied for 30 days. After this period, levels of cytokines IFN-gamma, IL-12, TNF-alpha and TGF-beta were measured. After blood collection, mice were perfused and the brains were submitted to immunohistochemistry for perineuronal net (PNN) evaluation and cyst quantification. The results showed that C57BL/6 mice presented higher levels of TNF-alpha and IL-12, while the levels of TGF-beta were similar between the two mouse lineages, associated with the elevated number of tissue cysts, with a higher occurrence of cysts in the posterior area of the PSC when compared to BALB/c mice, which presented a more homogeneous cyst distribution. Immunohistochemistry analysis revealed a greater loss of PNN labeling in C57BL/6 animals compared to BALB/c. These data raised a discussion about the ability of T. gondii to stimulate a systemic inflammatory response capable of indirectly interfering in the brain structure and function.

Automated summary

This study evaluated the effects of Toxoplasma gondii infection on the systemic inflammatory response and structure of the primary somatosensory cortex (PSC). The results showed increased levels of pro-inflammatory cytokines and tissue cysts in the infected mice, as well as a loss of neuronal net labeling in the cortex.